Careers
Cancer is associated with an overall seven fold increased risk of thrombosis. The main mechanism by which platelet thrombi promote cancer, is by wrapping around circulating tumor cells and protecting them while in circulation and then promoting their attachment on the blood vessel walls of the capillary. Once attached, the tumor cells can then divide and grow to form a metastatic tumor. Since metastasis is the main cause of mortality in cancer, Verseon's thrombin inhibitors can block metastasis by blocking platelet thrombus formation.
Verseon has developed anti-thrombotics that exert their inhibitory effect on thrombin via a novel mechanism of action. In fact, Verseon’s compounds are the first small molecules shown to inhibit thrombin via a novel mechanism of action. This novel mechanism of action promises novel pharmacology and reduced bleeding liability necessary for oncology indications
Verseon's novel DTIs promise an entirely new method of treating many types of solid tumor cancers such as breast, prostate, and others.
Angiogenesis is the formation of new blood vessels. Cancerous tumors usurp the natural process of angiogenesis in order to build the blood vessels needed to obtain the oxygen and nutrients to fuel their growth. By preventing blood vessel formation, anti-angiogenesis drugs starve cancerous tumors and inhibit their progress.
Verseon has developed two families of compounds that inhibit blood vessel growth without being generally toxic for surrounding cells. Additionally, Verseon's compounds do not exert their anti-angiogenic effect by binding to VEGF, the most common mechanism targeted by competing drugs and as such represent a new class of angiogenesis inhibitors.
Antithrombotics prevent blood from clotting and help treat a wide spectrum of diseases ranging from deep vein thrombosis, pulmonary embolism, myocardial infarction and ischemic stroke. With the introduction of the first generation of oral once‐a‐day antithrombotics, the annual world market for such drugs is predicted to reach $24 billion per year, growing from just $6.5 billion in 2001.
A New Class of Inhibitors
Verseon has designed a class of compounds that inhibit thrombin through a novel mechanism of action. These compounds present a unique coagulation and dose response profile in functional assays and promise much lower bleeding liability than that of current drugs. As such, these compounds constitute a novel class of pharmacological therapeutics.
Most thrombin active site inhibitors, such as argatroban and dabigatran, are substrate‐derived and rely on the highly basic guanidine or benzamidine motifs for activity. Verseon's inhibitors are structurally unique in that they do not incorporate either of these moieties. Although it has been well established that the guanidine and benzamidine groups can impart excellent affinity for thrombin, their use often comes at a high cost of poor oral bioavailability. For example argatroban, which was approved by the FDA in 2000, must be administered intravenously due to its very poor oral bioavailability, minimizing its therapeutic potential. While the profile for dabigatran is somewhat improved, oral administration still requires the offending groups be masked in the double prodrug dabigatran etexilate (Pradaxa), which manages to only reach a poor oral bioavailability of 3-7%.
Verseon has a growing product pipeline and is actively evaluating potential targets for future development.
| Discovery | Development | Preclinical | Phase 1 | Phase 2 | Phase 3 | |
| Thrombosis | ||||||
| Angiogenesis | ||||||
| Cervical Cancer | ||||||
| Alzheimer's | ||||||
Verseon's drug discovery platform is applicable to any clinical target with a known protein structure and as such provides the company with great program flexibility.
Programs in Verseon's pipeline typically fulfill the following criteria:
- Unmet market need
- Available target structure
- Tractable preclinical and clinical endpoints
Verseon has a growing product pipeline and is actively evaluating potential targets for future development.
| Discovery | Development | Preclinical | Phase 1 | Phase 2 | Phase 3 | |
| Thrombosis | ||||||
| Metastasis | ||||||
| Angiogenesis | ||||||